The Functional Advantages of Protein Oligomerization

Evolution Creates Evolution

As I have discussed many times, a single, run-of-the-mill, protein is beyond evolutionary explanation. The fitness landscape in protein sequence space is typically rugged, with occasional spikes representing protein designs. The resources required to evolve even a relatively simple protein exceed what evolution has available by at least 27 orders of magnitude. And that is generous as it comes from studies done by evolutionists. But proteins cause many more problems for evolution beyond their initial origin. For instance, something like a third of proteins form oligomers—protein machines consisting multiple subunits that bind together. Hemoglobin, for example, consists of four units, two alpha chains and two beta chains. Each chain is roughly 140 amino acids long. Michael Behe showed in his book The Edge of Evolution that the origin of simply the oligomeric interfaces is beyond evolutionary explanation. But again, the problems do not stop there. Even if evolution could somehow oligomerize proteins, what would happen then?

Oligomers may be homogeneous, consisting of repeats of the same subunit, or they may be heterogeneous, consisting of different subunits. Either way, it is unlikely that if evolution were somehow get lucky and not only construct proteins, but oligomerize them, that some great new function would arise. If so, it would represent a great amount of serendipity, for the new function would have been a lucky result. Imagine combining a few shovels to get a windmill.

But if there was no new function, then what would be the value of the new oligomer? The problem is not that evolutionists have no idea, but rather that they have too many ideas, none of which make sense. Here are six potential functional advantages that oligomerization may confer, as summarized in a review paper:

(1) More complex scaffolds may better support function, for example, by the introduction of a new active site at the interface between subunits. It has been estimated that roughly one sixth of oligomeric enzymes has an active site located at the inter-subunit interface.
(2) Oligomeric proteins can be allosterically regulated, introducing an additional level of control.
(3) There is a greater likelihood of an error-free transcript in a shorter protein sequence. A large protein composed of multiple, short, subunits, is more likely to be synthesized without errors than a single chain protein of comparable size.
(4) Where the monomer and oligomer differ in activity, additional regulatory flexibility may be achieved by regulating the conditions of oligomerization.
(5) Oligomeric proteins may be subjected to amplified evolutionary pressures, as deleterious mutations may be more pronounced and thus removed sooner from the gene pool. Conversely, the advantages of beneficial mutations may also be made evident sooner.
(6) Larger proteins are more resistant to degradation and denaturation. Indeed, an increase in oligomerization state is one of the protein stabilization strategies observed in thermophilic organisms.

Evolutionists are deeply wedded to teleological thinking. They have also constructed a theory full of serendipity. This summary is an example of both these trends, which often go together.

These six functional advantages imagined by evolutionists do not represent immediate improvements. For example, the second entry states that “oligomeric proteins can be allosterically regulated, introducing an additional level of control.” But immediately upon oligomerization, there would be no such regulation.

In fact, that is a generous understatement. For the evolution of allosteric regulation is far beyond evolution’s resources. The point here is that these imagined functional advantages of oligomerization call for an enormous helping of serendipity. Evolution creates X, which then enables some later evolutionary step to be taken. In this case, oligomerization is supposed to have assisted in the evolution of allosteric regulation.

Or again, the fifth entry states that “oligomeric proteins may be subjected to amplified evolutionary pressures.” Forget about the possible instabilities this could introduce, it apparently makes for a superior evolutionary process. So again, we have evolution constructing X, which then makes for better evolution. In short, evolution creates evolution.

Religion drives science, and it matters.

Finally, the Details of How Proteins Evolve

A Step-By-Step Description

How did proteins evolve? It is a difficult question because, setting aside many other problems, the very starting point—the protein-coding gene—is highly complex. A large number of random mutations would seem to be required before you have a functional protein that helps the organism. Too often such problems are solved with vague accounts of “adaptations” and “selection pressure” doing the job. But this week researchers at the University of Illinois announced ground-breaking research that provides a step-by-step, detailed, description of the evolution of a new protein-coding gene and associated regulatory DNA sequences. The protein in question is a so-called “antifreeze” protein that keeps the blood of Arctic codfish from freezing, and the new research provides the specific sequence of mutations, leading to the new gene. It would be difficult to underestimate the importance of this research. It finally provides scientific details answering the age-old question of how nature’s massive complexity could have arisen. As the paper triumphantly declares, “Here, we report clear evidence and a detailed molecular mechanism for the de novo formation of the northern gadid (codfish) antifreeze glycoprotein (AFGP) gene from a minimal noncoding sequence.” Or as lead researcher, professor Christina Cheng, explained, “This paper explains how the antifreeze protein in the northern codfish evolved.” This is a monumental finding. Having the scientific details, down to the level of specific mutations, of how a new protein-coding gene evolved—not from a related gene but from non-coding DNA—is something evolutionists could only dream of only a few short years ago. There’s only one problem: it is all junk science.

The first problem is that this new “research” is, in actuality, a just-so story:

In science and philosophy, a just-so story is an unverifiable narrative explanation for a cultural practice, a biological trait, or behavior of humans or other animals. The pejorative nature of the expression is an implicit criticism that reminds the hearer of the essentially fictional and unprovable nature of such an explanation. Such tales are common in folklore and mythology.

For example, the antifreeze protein is of relatively low complexity chiefly consisting a repeating sequence of three amino acids (threonine-alanine-alanine), and the evolutionists claim that these repeating sequences “strongly suggest” that the protein-coding gene “evolved from repeated duplications of an ancestral 9-nucleotide threonine-alanine-alanine-coding element.”

Why is that true?

Why does a repeating genetic sequence “strongly suggest” that it “evolved from repeated duplications?” What experiment revealed this truth? What evidence gives us this profound principle? The answer, of course, is that there is none. Nowhere do the evolutionists justify this claim because there is no empirical justification.

There is no scientific evidence for it. Zero.

The paper continues with yet more non-empirical claims. Those nine nucleotides “likely originated within a pair of conserved 27-nucleotide” segments that flank each side of the repetitive region. And these four 27-nucleotide segments are similar to each other, “indicating they resulted from the duplication of an initial copy.” As the paper concludes, “chance duplications” of an ancestral 27-nucleotide segment “produced four tandem copies.”

But why are those claims true? Why do such similarities imply an origin via evolutionary mechanisms? The problem is, they don’t. There is no empirical evidence for any of this. This is completely evidence-free.

The evolutionists next explain that the 9-nucleotide segment duplicated a large number of times because it worked well:

We hypothesize that, upon the onset of selective pressure from cold polar marine conditions, duplications of a 9-nt ancestral element in the midst of the four GCA-rich duplicates occurred.

The above quote is an example of the non-empirical, teleology that pervades evolutionary thought. It was upon the onset of cold conditions that the needed genetic duplications occurred. This is not empirical; this is story-telling.

The paper continues with a series of one-time, contingent events crucial to their story and non-empirical claims. The genetic sequence “was appropriately delimited by an existing in-frame termination codon.”

Appropriately delimited?

The presence of a region in two of the species “indicates that it existed in the gadid ancestor before the emergence of the AFGP.” The absence of a thymine nucleotide at a location in some of the species “very likely resulted from a deletion event,” causing a fortuitous frameshift which supplied the crucial signal peptide segment, telling cellular machinery that the protein should be secreted to the bloodstream. As the paper concludes, “the emerging AFGP gene was thus endowed with the necessary secretory signal.”

Endowed with the necessary signal?

There is no empirical evidence for any of this.

Another problem with this just-so account, is the substantial level of serendipity required. The new antifreeze protein did not arise from some random DNA sequence, but rather from crucial, preexisting segments of DNA that just happened to be lying around. In other words, the fish were facing a colder environment, they needed some antifreeze in their blood, and the pieces needed for such an antifreeze gene were fortuitously available.

The authors hint at this serendipity when they conclude that their story of how this protein evolved is an example of “evolutionary ingenuity.”

Evolutionary ingenuity?

The press release is even more revealing. Cheng admits that the evolution of this gene “occurred as a result of a series of seemingly improbable, serendipitous events.” For “not just any random DNA sequence can produce a viable protein.” Furthermore, in addition to the gene itself, “several other serendipitous events occurred.”

The DNA was “edited in just the right way,” and “somehow, the gene also obtained the proper control sequence that would allow the new gene to be transcribed into RNA.”

Even the evolutionists admit to the rampant serendipity. Nonetheless they are triumphant, for “the findings offer fresh insights into how a cell can invent ‘a new, functional gene from scratch.’”

Fresh insights?

In actuality the findings arose from a series of non-empirical claims.

Religion drives science, and it matters.

Rewrite the Textbooks (Again), Origin of Mitochondria Blown Up

There You Go Again

Why are evolutionists always wrong? And why are they always so sure of themselves? With the inexorable march of science, the predictions of evolution, which evolutionists were certain of, just keep on turning out false. This week’s failure is the much celebrated notion that the eukaryote’s power plant—the mitochondria—shares a common ancestor with the alphaproteobacteria. A long time ago, as the story goes, that bacterial common ancestor merged with an early eukaryote cell. And these two entities, as luck would have it, just happened to need each other. Evolution had just happened to create that early bacterium, and that early eukaryote, in such a way that they needed, and greatly benefited from, each other. And, as luck would have it again, these two entities worked together. The bacterium would just happen to produce the chemical energy needed by the eukaryote, and the eukaryote would just happen to provide needed supplies. It paved the way for multicellular life with all of its fantastic designs. There was only one problem: the story turned out to be false.

The story that mitochondria evolved from the alphaproteobacteria lineage has been told with great conviction. Consider the Michael Gray 2012 paper which boldly begins with the unambiguous truth claim that “Viewed through the lens of the genome it contains, the mitochondrion is of unquestioned bacterial ancestry, originating from within the bacterial phylum α-Proteobacteria (Alphaproteobacteria).”

There was no question about it. Gray was following classic evolutionary thinking: similarities mandate common origin. That is the common descent model. Evolutionists say that once one looks at biology through the lens of common descent everything falls into place.

Except that it doesn’t.

Over and over evolutionists have to rewrite their theory. Similarities once thought to have arisen from a common ancestor turn out to contradict the common descent model. Evolutionists are left having to say the similarities must have arisen independently.

And big differences, once thought to show up only in distant species, keep on showing up in allied species.

Biology, it turns out, is full of one-offs, special cases, and anomalies. The evolutionary tree model doesn’t work.

Now, a new paper out this week has shown that the mitochondria and alphaproteobacteria don’t line up the way originally thought. That “unquestioned bacterial ancestry” turns out to be, err, wrong.

The paper finds that mitochondria did not evolve from the currently hypothesized alphaproteobacterial ancestor, or from “any other currently recognized alphaproteobacterial lineage.”

The paper does, however, make a rather startling claim. The authors write:

our analyses indicate that mitochondria evolved from a proteobacterial lineage that branched off before the divergence of all sampled alphaproteobacteria.

Mitochondria evolved from a proteobacterial lineage, predating the alphaproteobacteria?

That is a startling claim because, well, simply put there is no evidence for it. The lack of evidence is exceeded only by the evolutionist’s confidence. Note the wording: “indicate.”

The evolutionist’s analyses indicate this new truth.

How can the evolutionists be so sure of themselves in the absence of literally any evidence?

The answer is, because they are evolutionists. They are completely certain that evolution is true. And since evolution must be true, the mitochondria had to have evolved from somewhere. And the same is true for the alphaproteobacteria. They must have evolved from somewhere.

And in both cases, that somewhere must be the earlier proteobacterial lineage. There are no other good evolutionary candidates.

Fortunately this new claim cannot be tested (and therefore cannot be falsified), because the “proteobacterial lineage” is nothing more than an evolutionary construct. Evolutionists can search for possible extant species for hints of a common ancestor with the mitochondria, but failure to find anything can always be ascribed to extinction of the common ancestor.

This is where evolutionary theory often ends up: failures ultimately lead to unfalsifiable truth claims. Because heaven forbid we should question the theory itself.

Religion drives science, and it matters.

New Ideas on the Evolution of Photosynthesis Reaction Centers

Pure Junk

Evolutionists do not have a clear understanding of how photosynthesis arose, as evidenced by a new paper from Kevin Redding’s laboratory at Arizona State University which states that:

After the Type I/II split, an ancestor to photosystem I fixed its quinone sites and then heterodimerized to bind PsaC as a new subunit, as responses to rising O2 after the appearance of the oxygen-evolving complex in an ancestor of photosystem II. These pivotal events thus gave rise to the diversity that we observe today.

That may sound like hard science to the uninitiated, but it isn’t.

The Type I/II split is a hypothetical event for which the main evidence is the belief that evolution is true. In fact, according to the science, it is astronomically unlikely that photosynthesis evolved, period.

And so, in typical fashion, the paper presents a teleological (“and then structure X evolved to achieve Y”) narrative to cover over the absurdity:

and then heterodimerized to bind PsaC as a new subunit, as responses to rising O2 …

First, let’s reword that so it is a little clearer: The atmospheric oxygen levels rose and so therefore the reaction center of an early photosynthesis system heterodimerized in order to bind a new protein (which helps with electron transfer).

This is a good example of the Aristotelianism that pervades evolutionary thought. This is not science, at least in the modern sense. And as usual, the infinitive form (“to bind”) provides the telltale sign. In other words, a new structure evolved as a response to X (i.e., as a response to the rising oxygen levels) in order to achieve Y (i.e., to achieve the binding of a new protein, PsaC).

But it gets worse.

Note the term: “heterodimerized.” A protein machine that consists of two identical proteins mated together is referred to as a “homodimer.” If two different proteins are mated together it is a “heterodimer.” In some photosynthesis systems, at the core of the reaction center is a homodimer. More typically, it is a heterodimer.

The Redding paper states that the ancient photosynthesis system “heterodimerized.” In other words, it switched, or converted, the protein machine from a homodimer to a heterodimer (in order to bind PsaC). The suffix “ize,” in this case, means to cause to be or to become. The ancient photosynthesis system caused the protein machine to become a heterodimer.

Such teleology reflects evolutionary thought and let’s be clear—this is junk science. From a scientific perspective there is nothing redeeming here. It is pure junk.

But it gets worse.

These pivotal events thus gave rise to the diversity that we observe today.

Or as the press release described it:

Their [reaction centers’] first appearance and subsequent diversification has allowed photosynthesis to power the biosphere for over 3 billion years, in the process supporting the evolution of more complex life forms.

So evolution created photosynthesis which then, “gave rise to” the evolution of incredibly more advanced life forms. In other words, evolution climbed an astronomical entropic barrier and created incredibly unlikely structures which were crucial for the amazing evolutionary history to follow.

The serendipity is deafening.

Religion drives science, and it matters.

Andreas Wagner: Genetic Regulation Drives Evolutionary Change

A Hall of Mirrors

A new paper from Andreas Wagner and co-workers argues that a key and crucial driver of evolution is changes to the interaction between transcription factor proteins and the short DNA sequences to which they bind. In other words, evolution is driven by varying the regulation of protein expression (and a particular type of regulation—the transcription factor-DNA binding) rather than varying the structural proteins themselves. Nowhere does the paper address or even mention the scientific problems with this speculative idea. For example, if evolution primarily proceeds by random changes to transcription factor-DNA binding, creating all manner of biological designs and species, then from where did those transcription factors and DNA sequences come? The answer—that they evolved for some different, independent, function; itself an evolutionary impossibility—necessitates astronomical levels of serendipity. Evolution could not have had foreknowledge. It could not have known that the emerging transcription factors and DNA sequence would, just luckily, be only a mutation away from some new function. This serendipity problem has been escalating for years as evolutionary theory has repeatedly failed, and evolutionists have applied ever more complex hypotheses to try to explain the empirical evidence. Evolutionists have had to impute to evolution increasingly sophisticated, complex, higher-order, mechanisms. And with each one the theory has become ever more serendipitous. So it is not too surprising that evolutionists steer clear of the serendipity problem. Instead, they cite previous literature as a way of legitimizing evolutionary theory. Here I will show examples of how this works in the new Wagner paper.

The paper starts right off with the bold claim that “Changes in the regulation of gene expression need not be deleterious. They can also be adaptive and drive evolutionary change.” That is quite a statement. To support it the paper cites a classic 1975 paper by Mary-Claire King and A. C. Wilson entitled “Evolution at two levels in humans and chimpanzees.” The 1975 paper admits that the popular idea and expectation that evolution occurs by mutations in protein-coding genes had largely failed. The problem was that, at the genetic level, the two species were too similar:

The intriguing result, documented in this article, is that all the biochemical methods agree in showing that the genetic distance between humans and the chimpanzee is probably too small to account for their substantial organismal differences.

Their solution was to resort to a monumental shift in evolutionary theory: evolution would occur via the tweaking of gene regulation.

We suggest that evolutionary changes in anatomy and way of life are more often based on changes in the mechanisms controlling the expression of genes than on sequence changes in proteins. We therefore propose that regulatory mutations account for the major biological differences between humans and chimpanzees.

In other words, evolution would have to occur not by changing proteins, but by changing protein regulation. What was left unsaid was that highly complex, genetic regulation mechanisms would now have to be in place, a priori, in order for evolution to proceed.

Where did those come from?

Evolution would have to create highly complex, genetic regulation mechanisms so that evolution could occur.

Not only would this ushering in of serendipity to evolutionary theory go unnoticed, it would, incredibly, be cited thereafter as a sort of evidence, in its own right, showing that evolution occurs by changes to protein regulation.

But of course the 1975 King-Wilson paper showed no such thing. The paper presupposed the truth of evolution, and from there reasoned that evolution must have primarily occurred via changes to protein regulation. Not because anyone could see how that could occur, but because the old thinking—changes to proteins themselves—wasn’t working.

This was not, and is not, evidence that changes in the regulation of gene expression can be “adaptive and drive evolutionary change,” as the Wagner paper claimed.

But this is how the genre works. The evolution literature makes unfounded claims that contradict the science, and justifies those claims with references to other evolution papers which do the same thing. It is a web of deceit.

Ultimately it all traces back to the belief that evolution is true.

The Wagner paper next cites a 2007 paper that begins its very first sentence with this unfounded claim:

It has long been understood that morphological evolution occurs through alterations of embryonic development.

I didn’t know that. And again, references are provided. This time to a Stephen Jay Gould book and a textbook, neither of which demonstrate that “morphological evolution occurs through alterations of embryonic development.”

These sorts of high claims by evolutionists are ubiquitous in the literature, but they never turn out to be true. Citations are given, and those in turn provide yet more citations. And so on, in a seemingly infinite hall of mirrors, where monumental assertions are casually made and immediately followed by citations that simply do the same thing.

Religion drives science, and it matters.

IC: We Can Say It, But You Can’t

Pre Adaptation

In contrast [to trait loss], the gain of genetically complex traits appears harder, in that it requires the deployment of multiple gene products in a coordinated spatial and temporal manner. Obviously, this is unlikely to happen in a single step, because it requires potentially numerous changes at multiple loci.

If you guessed this was written by an Intelligent Design advocate, such as Michael Behe describing irreducibly complex structures, you were wrong. It was evolutionist Sean Carroll and co-workers in a 2007 PNAS paper.

When a design person says it, it is heresy. When an evolutionist says it, it is the stuff of good solid scientific research.

The difference is the design person assumes a realist view (the genetically complex trait evinces design) whereas the evolutionist assumes an anti-realist view (in spite of all indications, the genetically complex trait must have arisen by blind causes).

To support their position, evolutionists often appeal to a pre adaptation argument. This argument claims that the various sub components (gene products, etc.), needed for the genetically complex trait, were each needed for some other function. Therefore, they evolved individually and independently, only later to serendipitously fit together perfectly and, in so doing, form a new structure with a new function that just happened to be needed. As Richard Dawkins once put it:

The bombardier beetle’s ancestors simply pressed into different service chemicals that already happened to be lying around. That’s often how evolution works.

The problem, of course, is that this is not realistic. To think that each and every one of the seemingly unending, thousands and thousands, of genetically complex traits just happened to luckily arise from parts that just happened to be lying around, is to make one’s theory dependent on too much serendipity.

Religion drives science, and it matters.

Blindness in Cave Fish is Due to Epigenetics

Evolutionists Say “We See”

A recent paper out of Brant Weinstein’s and William Jeffery’s laboratories on eye development, or the lack thereof, in blind cave fish has important implications for evolutionary theory (paper discussed here). The study finds that the loss of eyes in fish living in dark Mexican caves is not due to genetic mutations, as evolutionists have vigorously argued for many years, but due to genetic regulation. Specifically, methylation of key development genes represses their expression and with it eye development in this venerable icon of evolution. But the finding is causing yet more problems for evolutionary theory.

Darwin appealed to the blind cave fish in his one long argument for evolution. It is a curious argument in many ways, and the first sign of problems was in Darwin’s presentation where he flipped between two different explanations. At one point he explained the loss of vision in the cave fish as an example of evolutionary change not due to his key mechanism, natural selection. Instead, the Sage of Kent resorted to using the Lamarckian mechanism or law of “use and disuse.” Privately Darwin despised and harshly criticized Lamarck, but when needed he occasionally employed his French forerunner’s ideas.

Elsewhere Darwin hit upon a natural selection-based mechanism for the blind cave fish, explaining that elimination of the costly and unneeded vision system would surely raise the fitness of the hapless creatures.

This latter explanation would become a staple amongst latter day evolutionary apologists, convinced that it mandates the fact of evolution. Anyone who has discussed or debated evolutionary theory with today’s Epicureans has likely encountered this curious argument that because blind cave fish lost their eyes, therefore the world must have arisen by itself.

Huh?

To understand the evolutionary logic, or lack thereof, one must understand the history of ideas, and in particular the idea of fixity, or immutability, of species. According to evolutionists, species are either absolutely fixed in their designs, or otherwise there are no limits to their evolutionary changes and the biological world, and everything else for that matter, spontaneously originated.

Any evidence, for any kind of change, no matter how minor, is immediately yet another proof text for evolution, in all that the word implies.

Of course, from a scientific perspective, the evidence provides precisely zero evidence for evolution. Evolution requires the spontaneous (i.e., by natural processes without external input) creation of an unending parade of profound designs. The cave fish evidence shows the removal, not creation, of such a design.

The celebration of such evidence and argument by Darwin and his disciples reveals more about evolutionists than evolution. That they would find this argument persuasive reveals their underlying metaphysics and the heavy lifting it performs. It is all about religion.

We are reminded of all this with the news of Weinstein’s new study. But we also see something new: The insertion, yet again, of Lamarck into the story. The irony is that the epigenetics, now revealed as the cause of repressed eye development in the cave fish, hearkens back to Lamarck.

Darwin despised Lamarck and later evolutionists made him the third rail in biology. Likewise they have pushed back hard against the scientific findings of epigenetics and their implications.

The environment must not drive biological change.

False.

Well such biological change must not be transgenerational.

False.

Well such inheritance must not be long lasting, or otherwise robust.

False again.

This last failure is revealed yet again in the new blind cave fish findings.

False predictions count. A theory that is repeatedly wrong, over and over, in all of its fundamental expectations, will eventually be seen for what it is.

The rise of epigenetics is yet another such major failure. Evolutionists pushed back against it because it makes no sense on the theory, and that means it cannot now be easily accommodated.

One problem is that epigenetics is complex. The levels of coordination and intricacy of mechanism are far beyond evolution’s meager resources.

It’s not going to happen.

Another problem is the implied serendipity. For instance, one epigenetic mechanism involves the molecular tags places on the tails of the DNA packing proteins called histones. While barcoding often seems to be an apt metaphor for epigenetics, the tagging of histone tails can influence the histone three dimensional structures. It is not merely an information-bearing barcode. Like the tiny rudder causing the huge ship to change course, the tiny molecular tag can cause the much larger packing proteins to undergo conformational change, resulting in important changes in gene accessibility and expression.

This is all possible because of the special, peculiar, structure and properties of the histone protein and its interaction with DNA. With evolution we must believe this just happened to evolve for no reason, and thus fortuitously enabled the rise of epigenetics.

Another problem with epigenetics is that it is worthless, in evolutionary terms that is. The various mechanisms that sense environmental shifts and challenges, attach or remove one of the many different molecular tags to one of the many different DNA or histone locations, propagate these messages across generations, and so forth, do not produce the much needed fitness gain upon which natural selection operates.

The incredible epigenetics mechanisms are helpful only at some yet to be announced future epoch when the associated environmental challenge presents itself. In the meantime, selection is powerless and according to evolution the incredible system of epigenetics, that somehow just happened to arise from a long, long series or random mutations, would wither away with evolution none the wiser.

These are the general problems with epigenetics. In the case of the blind cave fish, however, there is possible explanation. It is a longshot, but since this case specifically involves the loss of a stage of the embryonic development, evolutionists can say that genetic mutations caused changes in the methylating proteins, causing them to be overactive.

This explanation relies on the preexistence of the various epigenetic mechanisms, so does not help to resolve the question of how they could have evolved. What the explanation does provide is a way for evolutionists to dodge the bullet presented by the specter of the cave fish intelligently responding to an environmental shift.

Such teleology in the natural world is not allowed.

So the evolutionary prediction is that these proteins will be found to have particular random changes causing an increase in their methylation function, in particular at key locations in key genes (i.e., the genes associated eye development).

That’s a long shot, and an incredible violation of Occam’s Razor.

My predictions are that (i) this evolutionary prediction will fail just as the hundreds that came before, and (ii) as with those earlier failures, this failure will do nothing to open the evolutionist’s eyes.

Religion drives science, and it matters.

Repetitive Elements: Evolution Has a Toolkit, And Several Other Findings

Tightly Coupled Molecular Machines Make Evolution Work

I’m not an expert carpenter, but if I know what needs to be built I’ll eventually get there. It may not be beautiful, but given a blueprint I can build a structure. What if I didn’t have that blueprint? What if I had no idea what needed to be built—no notion of where the task was headed? Furthermore, what if I had no knowledge of structures in general. Just randomly cutting wood and pounding nails probably would not end well. This is the elephant in the room for evolution, for according to evolutionary theory, random actions are precisely what built the world. It is what the Epicureans claimed two thousand years ago, and this random-creation hypothesis fares no better today than it did then. In fact, with the findings of modern science we now know far more about the details than did the Epicureans, and it has just gotten worse for their hypothesis. This is why evolutionists, as we have repeatedly documented, consistently appeal to teleological language. Regulatory genes “were reused to produce different functions,” Dinosaurs “were experimenting” with flight, and the genome was “designed by evolution to sense and respond.” Such Aristotelianism, which casts evolution as an intelligent process working toward a goal, makes the story more palatable; after all, evolution had a blueprint in mind. All of this makes for a glaring internal contradiction: on the one hand evolution has goals; yet on the other hand evolution is a mindless, mechanical process driven by random, chance events. As Jernej Ule explained last week:

We’re all here because of mutations. Random changes in genes are what creates variety in a species, and this is what allows it to adapt to new environments and eventually evolve into completely new species.

This makes evolution, rather inconveniently, dependent on random events (no, natural selection doesn’t change this—it cannot coax the right mutations to occur) which, by definition, do not work towards a goal—they do not build anything:

This ambiguity creates a great challenge. On the one hand, mutations are needed for biological innovation, and on the other hand they cause diseases.

Indeed. This is not looking good. As one Michael Skinner recently explained:

the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed. Scientists, well-aware of the issue, have proposed a variety of genetic mechanisms to compensate: genetic drift, in which small groups of individuals undergo dramatic genetic change; or epistasis, in which one set of genes suppress another, to name just two. Yet even with such mechanisms in play, genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change [between species if evolution is true] for a host of traits, from adjustments in metabolism to resistance to disease.

Whereas Skinner appealed to epigenetics to save the theory, Ule appeals to repetitive elements. Evidence has shown that far from being “junk DNA,” repetitive elements plays a genetic regulatory role. As a result evolutionists such as Ule have concluded repetitive elements “are an important toolkit for evolution.”

Like any good carpenter, evolution has a toolkit.

Ule and his co-workers are now elaborating on the details of how repetitive element toolkit might work. It goes like this: (i) Random mutations gradually modify repetitive elements, (ii) these repetitive elements are sometimes incorporated as part of the blueprint instructions for making a protein, (iii) there are several complicated molecular machines that either repress or allow such incorporation of these repetitive elements in the blueprint.

According to Ule, this complicated process, including these two opposing machines which are “tightly coupled,” allows evolution to experiment and successfully evolve more complicated species, such as humans:

We’ve known for decades that evolution needs to tinker with genetic elements so they can accumulate mutations while minimising disruption to the fitness of a species. … This [process we have discovered] allows the Alu elements to remain in a harmless state in our DNA over long evolutionary periods, during which they accumulate a lot of change via mutations. As a result, they become less harmful and gradually start escaping the repressive force. Eventually, some of them take on an important function and became indispensable pieces of human genes. To put it another way, the balanced forces buy the time needed for mutations to make beneficial changes, rather than disruptive ones, to a species. And this is why evolution proceeds in such small steps – it only works if the two forces remain balanced by complementary mutations, which takes time. Eventually, important new molecular functions can emerge from randomness.

These suggestions from Skinner and Ule are the latest in a long, long line of ideas evolutionists have come up with, in an attempt to make sense of their random creation hypothesis. In modern evolutionary thought, the first such idea was natural selection.

The reason there is a long, long line of ideas is none of them work. They are becoming ever more complicated, ever more unlikely, and equally useless in solving the basic problem of random events constructing the world.

But Ule’s latest attempt highlights yet another problem: serendipity. All of the solutions, from natural selection on up to epigenetics and repetitive elements rely on serendipity, and this reliance is increasing. Ule’s solution is serendipity on steroids, for the idea holds that evolution just happened to create (i) repetitive elements, and (ii) the complicated, finely-tuned, opposing molecular machines that repress or allow those repetitive elements into the protein instructions.

This isn’t going to work, but the point here is that even if it did somehow work, it amounts to evolution creating evolution. In order for evolution to have created so many of the species, it first must have lucked into creating these incredible mechanisms, which then in turn allowed evolution to occur. And all of this must have occurred with no foresight.

This is just silly. This violates the very basics of science. Imagine a car factory that uses highly complex machines, such as drill presses and lathes, to build the cars. Now imagine the factory first creating those machines by random chance, so then the cars could be built, by yet more random chance events.

Religion drives science, and it matters.

A Single Mutation Makes Humans

The fix Was In

When evolutionists found out that the chimp and human genomes were practically identical they went ape, claiming the evidence all but proved our shared lineage, with the chimp, to a small, primitive, ancestral primate. There was only one problem: With so few random genetic changes, how would such dramatic and complex changes come about? Far from a confirmation, our similar genes posed a dilemma for evolution. For how could so little genetic change cause so much significant evolutionary distance be traversed? And if the answer is, as it always seems to be, that those rare and random genetic changes were able to achieve such monumental results because the requisite parts and pieces that would be used were, fortuitously, already in place (because they just happened to have evolved for some other reason), then we have entered the realm of just-so stories. For the theory then amounts to the claim that “the fix was in.” The various key ingredients to making a human were all there, lying around, perhaps in disguise, or perhaps doing some other job. And then they were systematically recruited, coming into their own by virtue of a few, rare, mutations finally occurring and enabling the puzzle pieces to come together. It would be like a supersonic jet aircraft just happening to come together because its various parts just luckily were lying around. That is serendipity on steroids.

Well it just gets worse. More recently evolutionists were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.”

In fact the beneficial mutations in protein-coding genes, which presumably would be important in evolving the human from a small, primitive ape, literally number only in the hundreds. It would be astonishing if the human could be evolved from so few mutations.

But again, it just gets worse. For now evolutionists must conclude that not only are there few random mutations that must somehow create Newton and Einstein (to name just a couple of humans), and not only are most of those mutations neutral or slightly deleterious, and not only would evolution probably have only a few hundred genes undergoing selection, but that a monumental part of that evolutionary change, so important in creating humans, must have arisen from, yes, a single mutation. To wit:

What distinguishes humans from monkeys and apes? The gene ARHGAP11B is probably among the things that make humans special: This gene is only present in humans and contributes to the amplification of brain stem cells. Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden have now made a spectacular finding: It is a single base pair substitution in the ARHGAP11B gene that ultimately is responsible for the ability of the ARHGAP11B protein to amplify brain stem cells, a process thought to underlie the expansion of the neocortex in modern humans.

Spectacular indeed. As one of the researchers explained:

This change is tiny on a genomic scale but substantial in its functional and evolutionary consequences – it’s a single base substitution that likely drove brain size evolution and that may have set the stage for what makes humans special.

A single mutation? Here we have evolution reductio ad absurdum. A single mutation essentially worked the magic to create humans. How lucky we are.

Of course such absurdity entails the idea that an army of molecular components were serendipitously in place, ready and waiting for the single mutation to unleash their creative powers.

The fix was in.

How Did Birds Get Their Wings? Bacteria May Provide a Clue to the Genomic Basis of Evolutionary Innovation, Say Evolutionists

30 Days of Evolution

That evolution occurred is known to be a fact but how evolution occurred is not known. In particular we are ignorant of how evolutionary innovations arose. Of course biological novelties and innovations arose from a series of random chance events, but it is less than reassuring that we cannot provide more detail. How exactly did the most complex designs spontaneously arise? What mechanisms overcame, over and over, the astronomical entropy barriers, by sheer luck of the draw? As Craig MacLean’s and Andreas Wagner’s, and coworker’s, new PLOS Genetics paper begins, “Novel traits play a key role in evolution, but their origins remain poorly understood.” Could it be that evolution is not actually a fact? No, not according to evolutionists. And this new paper claims to provide the basis for how the seemingly impossible became the mundane.

The paper begins by summarizing the many proposed genetic mechanisms for the evolution of biological innovations:

An evolutionary innovation is a new trait that allows organisms to exploit new ecological opportunities. Some popular examples of innovations include flight, flowers or tetrapod limbs [1,2]. Innovation has been proposed to arise through a wide variety of genetic mechanisms, including: domain shuffling [3], changes in regulation of gene expression [4], gene duplication and subsequent neofunctionalization [5,6], horizontal gene transfer [7,8] or gene fusion [9]. Although innovation is usually phenotypically conspicuous, the underlying genetic basis of innovation is often difficult to discern, because the genetic signature of evolutionary innovation erodes as populations and species diverge through time.

1. Mayr E. Animal Species and Evolution. Cambridge: MA: Harvard University Press; 1963.

2. Pigliucci M. What, if anything, is an evolutionary novelty? Philos Sci. 2008;75: 887–898. Available:http://philpapers.org/rec/PIGWIA

3. Patthy L. Genome evolution and the evolution of exon-shuffling—a review. Gene. 1999;238: 103–14. Available: http://www.ncbi.nlm.nih.gov/pubmed/10570989 pmid:10570989

4. True JR, Carroll SB. Gene co-option in physiological and morphological evolution. Annu Rev Cell Dev Biol. 2002;18: 53–80. doi: 10.1146/annurev.cellbio.18.020402.140619. pmid:12142278

5. Zhang J. Evolution by gene duplication: An update. Trends Ecol Evol. 2003;18: 292–298. doi: 10.1016/S0169-5347(03)00033-8.

6. Bergthorsson U, Andersson DI, Roth JR. Ohno’s dilemma: evolution of new genes under continuous selection. Proc Natl Acad Sci U S A. 2007;104: 17004–9. doi: 10.1073/pnas.0707158104. pmid:17942681

7. Boucher Y, Douady CJ, Papke RT, Walsh DA, Boudreau MER, Nesbø CL, et al. Lateral gene transfer and the origins of prokaryotic groups. Annu Rev Genet. 2003;37: 283–328. doi: 10.1146/annurev.genet.37.050503.084247. pmid:14616063

8. Wiedenbeck J, Cohan FM. Origins of bacterial diversity through horizontal genetic transfer and adaptation to new ecological niches. FEMS Microbiol Rev. 2011;35: 957–976. doi: 10.1111/j.1574-6976.2011.00292.x. pmid:21711367

9. Thomson TM, Lozano JJ, Loukili N, Carrió R, Serras F, Cormand B, et al. Fusion of the human gene for the polyubiquitination coeffector UEV1 with Kua, a newly identified gene. Genome Res. 2000;10: 1743–56. pmid:11076860 doi: 10.1101/gr.gr-1405r

The unspoken problem here is, as usual, serendipity. The various proposed genetic mechanisms for the evolution of biological innovations all suggest an amazing bit of fortuitous luck. For random chance events just happened to create these various complicated structures and mechanisms (such as horizontal gene transfer and protein domains their shuffling) which then produced new evolutionary breakthroughs.

Evolution didn’t know what was coming. Evolution did not plan this out, it did not realize that horizontal gene transfer would lead the way to new biological worlds. The evolution of horizontal gene transfer would require a long sequence of random mutations, many of which would not provide any fitness advantage. And when the construction project was completed, and the first horizontal gene transfer capability was possible, there would be no immediate advantage.

This is because there would have been no genes to transfer. The mechanism works only when it is present in more than one, neighboring, cells. One cell gives, and another cells receives. By definition the mechanism involves multiple cells.

But it doesn’t stop there. Even if the first horizontal gene transfer capability was able to spread across a population, and even if it did provide a fitness advantage to the fortunate citizens, there would not be even a hint of the enormous world of biological innovations that had just been opened.

In other words, what this evolutionary narrative entails is monumental serendipity. Biological structures and mechanisms (horizontal gene transfer in this case, but it is the same story with the other hypotheses listed above) are supposed to have evolved as a consequence of a local, proximate, fitness advantage: a bacteria could now have a gene it didn’t have before.

But it just so happened that the new structures and mechanisms would also, as a free bonus, be just what was needed to produce all manner of biological innovations, far beyond assisting a lowly bacteria increase its fecundity.

This is monumental serendipity.

The science contradicts the theory

Undaunted, the new paper finds that one of the other mechanisms, gene duplication and subsequent neofunctionalization, is a key enabler and pathway to biological innovations.

That conclusion resulted from what otherwise was a fine piece of research work. The experimenters exposed different populations of Pseudomonas aeruginosa, a dangerous infectious bacteria, to 95 new sources of its favorite food: carbon.

The bacteria had to adjust to the new flavors of carbon and they did so with various genetic modifications, including various genetic mutations. In the most challenging cases (where the new carbon sources were most difficult for the bacteria to adjust to), the bacteria often produced mutations in genes involved in transcription and metabolism. And these mutations often occurred in genes where there were multiple copies, so the mutations occurred in one copy while the other copy could continue in its normal duties.

The problem is, these genetic duplicates were preexisting in the P. aeruginosa genome. This is yet another instance of serendipity.

Why? Because preexisting duplicates are not common. Only about 10% of the genes have duplicates lying around, and fortunately, the genes needed for adaptation (involving transcription and metabolism) just happened to have such duplicates.

Now there were a few instances of de novo gene duplication. That is, once the experiment began, and after the P. aeruginosa populations were exposed to the challenging diets, a total of six genes underwent duplication events. But in each and every case, the duplication events occurred repeatedly and independently, in different populations (for each of the 95 different carbon sources, the experimenters ran four parallel trials with independent populations).

This result indicates directed gene duplication. This is because it is highly unlikely that random, chance, gene duplication events just happened hit on the same gene in different populations. Here is an example calculation.

Let’s assume that in the course of the experiment, which ran for 30 days and about 140 generations of P. aeruginosa, some genes may undergo duplication events by chance. Next assume there is a particular gene that needs to be duplicated and modified in order to for P. aeruginosa to adapt to the new food source. (Note that there may be several such genes, but as we shall see that will not affect the conclusion). Given that there are four separate, independent trials, what is the probability that the gene will be duplicated in two or more of those trials?

Let P_dup be the probability that any gene is duplicated in the course of the experiment. For our gene of interest, it may be duplicated in 0, 1, 2, 3, or all 4 of the trials. The binomial distribution describes the probability, P, of each of these outcomes. To answer our question (i.e., What is the probability that the gene will be duplicated in two or more of those trials?) we sum the binomial distribution’s value for N = 2, 3 and 4. In other words, we calculate P(2) + P(3) + P(4).

This will give us the probability of observing what was observed in the experiment (i.e., the duplication events occurred repeatedly and independently, in different populations, in all 6 cases where duplication events were observed).

Well for a reasonable value of P_dup, the probability that any gene is duplicated in the course of the experiment, such as 0.0001, the probability of observing multiple duplications events for any given food source (i.e., P(2) + P(3) + P(4)) is about 60 in one billion, or 6  times 10^-8. Even worse, the probability of observing this in all 6 cases where duplication events were observed is about 5 times 10^-44.

It isn’t going to happen.

Exceptionally high rates of gene duplication, in particular genomic regions of Salmonella typhimurium, in a high growth rate medium, were observed to be about 0.001 and even slightly above 0.01 in rare cases.

If we go all out and set P_dup to an unrealistically high 0.1, our results are still unlikely. The P(2) + P(3) + P(4)) is .05, and the probability of observing this in all 6 cases where duplication events were observed is about 2 times 10^-8.

In order to raise these probabilities to reasonable levels, such that what was observed in the experiment is actually likely to have occurred, we need to raise P_dup to much higher values. For example, for a P_dup of .67 (two-thirds probability), P(2) + P(3) + P(4)) is .89, and the probability of observing this in all 6 cases where duplication events were observed is about .5.

But even this doesn’t work. For if we were to imagine unrealistically high P_dup values of 0.1 or higher, then massive numbers of duplication events would have been observed in the experiments.

But they weren’t.

Once again, the science contradicts the theory. Our a priori assumption that evolution is a fact, and that the P. aeruginosa adaptations to the new food sources were driven by random mutations, did not work. The theory led to astronomically low probabilities of the observed results.

What the observed gene duplications are consistent with is directed gene duplications. Just as mutations have been found to be directed in cases of environmental challenges, it appears that gene duplications may also be directed.

The paper’s premise, that biological innovations such as flowers and wings are analogous to bacteria adapting to new nutrient sources, is fallacious. But setting that aside, the experimental results do not make sense on evolution’s mechanism of random mutations and natural selection. Instead, the results indicate directed adaptation.

Name It / Claim It: Epigenetics Now Just Another Evolutionary Mechanism

In Spite of the Cognitive Dissonance

It is often said that all truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident. And so it is with epigenetics which evolutionists opposed and blackballed for a century before finally appropriating it as just another mode of evolutionary change. (see here, here, and here for more discussion of this history of misdirections regarding Lamarckism and epigenetics). Here is an example of evolutionists, after a century of denial and rejection, claiming epigenetics as their own.

Our example comes from this 2011 review paper on epigenetics in plants. Since plants are sessile they cannot simply move away from environmental challenges that occur. Therefore they need adaptation mechanisms. And since seeds are dispersed not too far from the parent plant, the next generation is likely to face the same environmental challenge. Therefore the adaptation mechanisms should be transgenerational, or heritable. Finally, since environmental challenge may be relatively short lived, lasting only a few generations, there is insufficient time for evolution by random mutations and natural selection to act. Therefore the adaptation mechanisms need to be fast-acting and reversible. These various requirements make epigenetics an “attractive alternative”:

The heritability of reversible epigenetic modifications that regulate gene expression without changing DNA sequence makes them an attractive alternative mechanism.

Note the design language. Not only are evolutionists naming and claiming the once evil epigenetics as just another mode of evolution, they also identify it as “an attractive alternative mechanism,” which is precisely how engineers discuss their design options.

Note, as we have discussed, the notion that such epigenetic mechanisms are just another mode of evolution makes no sense for several reasons. Unlike evolutionary change which is slow, epigenetics is fast. Unlike evolutionary change which propagates through the population from a single mutation occurring in a single individual, epigenetics works in parallel, occurring in many individuals across the population. Unlike evolutionary change which must come about by the selection of changes that must not be induced by the environment, epigenetics is induced by the environment. Unlike evolutionary change which generally is not repeatable, epigenetics is repeatable.

Furthermore, epigenetic mechanisms are, themselves, sophisticated designs. Their origin is far beyond evolution’s meager resources. Random mutations are not going to produce such directed adaptation mechanisms. And even if such a miracle were to occur, it would not survive, because it would not be selected for. This is because such mechanisms provide a differential reproductive advantage, and therefore a fitness improvement, not under the current conditions, but under some future, unforeseen conditions. There is no fitness improvement at the time of origin by random mutations.

There is a reason why evolutionists have so vehemently opposed this Lamarckian idea—it contradicts evolutionary theory. But like saltationism which was once rejected (by Darwin) due to its obvious implications, only to be guardedly accepted years later when the coast was clear (though it makes no sense on evolution), so too epigenetics must be accepted while downplaying the cognitive dissonance it forces on evolution.

Prehoda and Thornton Find New Levels of Serendipity

Evolution is Endlessly Falsified

A recent study out of the University of Oregon purports to show the evolutionary pathway of a key protein that helps to control the mitotic spindle, a structure inside the dividing cell that distributes the chromosomes to the daughter cells. In fact the research adds to a growing line of evidence destructive of evolutionary theory. Consider the following findings:

Transposable elements important in mammalian evolution

HGT plays key role in prokaryote and eukaryote evolution

Genetic regulation drives human evolution

Genetic regulation key in hominid evolution

Genetic regulation drove the evolution of the tetrapods

Genetic regulation important in the evolution of the metazoans

MicroRNA key to the evolution of land plants

Transposable elements and their repressor genes drove human evolution

Retroviruses played a crucial role human evolution

Alternative splicing drove evolution

Behavior drives evolution

A natural genetic engineering toolkit drove evolution

Key gene product evolved from several junk parts

What these various claims have in common is that large molecular structures were important causes of evolution. For example, the human and the chimpanzee have highly similar genes, so they did not evolve to be different by the usual explanation of random mutations modifying the genes. The human and chimpanzee do not differ at the level of the gene. Instead, they differ at higher, more complicated levels, such as in the regulation of those genes, which involves multiple molecular structures.

So evolutionists are forced to conclude that the genes required to build a human serendipitously evolved long before there were humans. After that, all that was needed were some changes to their regulation, and you had humans.

How lucky.

This story of serendipity, as indicated by the sampling of headlines above, has repeated itself over and over. In addition to genetic regulation, evolution was caused by transposable elements and their repressor genes, horizontal gene transfer mechanisms, micro RNAs, alternate splicing, retroviruses, behavior, and natural genetic engineering toolkits.

This is ludicrous. This is absurd. Evolutionists have been forced to make conclusions that are astronomically impossible.

Evolution must have constructed elaborate mechanisms and structures, in advance, which then became crucial agents of evolution, creating all kinds of biological wonders. Simply put, evolution must have created evolution. And in recent years such serendipity in the evolution narrative has skyrocketed. Evolution must have constructed elaborate mechanisms over, and over, and over.

Now, this latest research just adds more serendipity to the evolution narrative. Evolutionists are forced to conclude that a completely unrelated enzyme just happened to be highly similar to the key mitotic spindle protein. All that was required was a single mutation and, behold, the crucial mitotic spindle protein was created.

It would be finding a jet engine inside of clothing factory. Hey, we can use that for airplanes!

The scientific evidence contradicts evolution.

Natural Selection Does Machine Learning

It’s All Inevitable

After explaining the limitations of natural selection it is good to see the feature article in this week’s NewScientist admit that “current ways of thinking about evolution give a less-than-complete picture of how that [the spontaneous evolution of ‘all living things’] works.” Less-than-complete? That is evolution-speak for a theoretical meltdown. It’s no secret that the idea that the biosphere arose spontaneously is contradicted by the science. For evolutionists, that means their theory is “less-than-complete.” Well I suppose, technically, that is true. A theory that makes no sense is “less-than-complete.” Evolutionists are masters of the euphemism. They are also masters of the epicycle.

With each failure evolutionists modify and patch their theory with so many epicycles. Today the theory is enormously complex. And this NewScientist article provides one more example. The article explains the “less-than-complete” aspects of natural selection, and how it’s now all fixed. Yes, evolution was a fact, but now it’s even more of a fact. We were certain, but now we can be even more certain it is true.

Why? Because now natural selection has been expanded. Instead of just acting on genes, it acts on genetic regulatory processes—the incredibly complex networks of transcription factors and other molecular agents that help to regulate gene expression.

It turns out that if natural selection acts at the network level, everything works out as it should. We shouldn’t doubt this for, as evolutionists point out, it is analogous to the brain’s fancy techniques for learning.

In fact, natural selection is actually engaged in “deep learning,” a machine learning technique used on Big Data. As usual, strangely enough evolution mimics contemporary technology.

As we have discussed before, when the leading edge in biology was breeding, evolution was cast as a natural breeder. When computers became increasingly connected via networks, evolution was said to use “networks.” When artificial intelligence was thought to be on the horizon, evolution was said to use “molecular intelligence.” When the state of the art was genetic engineering, evolution is cast as a natural genetic engineer and “Biotechnology” was claimed as an evolutionary mechanism. So it is hardly surprising that now “Big Data” has been enlisted as yet another example of a cutting edge idea that fits right in with evolutionary theory. You see evolution is cool. It’s trendy and relevant. Whatever the latest technology is, it’s a perfect description of how evolution works.

As the article explains, evolution rests on three pillars: variation, natural selection and inheritance. And if natural selection uses machine learning techniques at the level of genetic regulation then, WaLa, we can now explain why evolution is such a good problem-solver, creating all sorts of complexity in such short order. In fact, it’s inevitable.

Of course there aren’t any actual biological details here. The results are obtained in the austere world of computer simulations, which evolutionists work hard at developing, debugging, and testing, to get just the right result. And those simulations are hosted on finely-tuned computers, running on loads of electricity, conveniently available in a wall socket.

And of course this new, high-tech, version of natural selection requires the pre existence of populations, functional, reproducing, organisms, heredity, and of course genetic regulation. No word on how all that arose, but we’re certain evolutionists will figure it out.

It’s inevitable.

Miracles are a Glaring Problem for Evolution, and Here’s Why

Begging the Question

A commenter recently reminded me of one of the many fundamental fallacies of evolutionary thought. When I point out problems with evolution, and make arguments against evolutionary thought, it is not because I am against the idea or want it to be false. Life would be much easier if the evidence simply supported evolution, if evolutionary thought was a stellar example of intellectual progress, if—to put it simply—evolution was an undeniable scientific fact, just as evolutionists insist. But it’s not. Evolution is not any of those. Evolution is not supported by the empirical evidence, it is not a rational, intellectual movement, and it is not a scientific fact, undeniable or otherwise. I’m not grinding a personal ax here, I’m simply pointing out the obvious. It makes no difference to me if evolution is true, false, or somewhere in between. But it does make a difference when we lie to ourselves.

One of the lies we tell ourselves is about miracles and how they relate to evolution. Specifically, evolutionists have been making arguments against miracles for centuries. A convenient starting place is seventeenth century church history, when Roman Catholic and Protestant elements of the church argued with each other, and between themselves, about miracles. It is a long story, but the upshot was that miracles were increasingly viewed with disdain for several reasons.

By the time David Hume arrived in the mid eighteenth century, the dust was settling. Hume is well known for his arguments against miracles, but he was largely repackaging sentiment that had long since been expressed.

Some arguments were epistemological. Others were theological, philosophical or ontological. But the short version is that evolutionary thought emerged in a milieu in which miracles were on the way out, both as explanatory mechanisms and as historical reality. Darwin contemporary David Friedrich Strauss, and his Life of Jesus, is but one of many examples of this broad, robust movement.

The movement against miracles was, not surprisingly, influential in the natural sciences. Simply put, if we’re not to appeal to miracles, then the world must have arisen naturalistically. This had a profound effect on the critical thinking, or lack thereof, of the time. Speculative hypotheses, with little basis in fact, enjoyed serious consideration and triumphant acceptance.

The bar was placed exceedingly low for such theories as pure conjecture became acceptable and celebrated science. Monumental scientific problems with the notion of spontaneous origins went ignored and evolutionary theories (from cosmological to biological) soon became “fact.”

Today strictly naturalistic, evolutionary, theories are a given. They simply are accepted as true, or as true as anything in science can be. And it also is a given that miracles are false. But what evolutionists prefer to overlook is that there is a causal relationship here. The latter made way for, and mandated, the former.

What an incredible coincidence it would be if, on the one hand, miracles were known to be false and, on the other hand, the empirical evidence turned out to prove a naturalistic origins. Theology, philosophy and science would have converged on the same truth.

But there is no such convergence.

The “convergence” that occurred is artificial. It is artificial because the empirical scientific evidence was interpreted according to the cultural mandate. Science was told what to do.

Indeed, from an objective, theory neutral, perspective, evolution is unlikely. It is not good science. In fact it is an outstanding example of bad science, breaking all the rules of what the textbooks tell us about how science is supposed to work. The idea that the multitude of species, the cosmos, consciousness and, well, everything, arose spontaneously by the interplay of chance contingencies of history and natural laws is silly. And that is being kind.

The problem of miracles is another example of the failure of evolutionary thought. Religion drives science, and it matters.

The Evolution of Neural Crest Cells: Teleology Raised to the Power of Serendipity

Early stem cells were set aside to create new features

There is a reason why Aristotle’s ideas persisted for thousands of years—they advance fundamental themes in how we think. And no, those ideas did not become outdated with the rise of modern science, as the textbooks explain. Consider a recent paper on the flight of bats which stated that the bat’s specialized airflow sensors evolved in order “to guide motor behaviors” and that vertebrate nervous systems, in general, “have flexibly adapted to accommodate anatomical specializations for flight.” The infinitive form is the key. Evolutionary theory is supposed to have rejected teleology. Whereas Aristotle explained natural phenomena as a consequence of final causes, modern science, so the textbooks state, is free of such mysteries. After Bacon it was all about empiricism, mathematical descriptions and natural laws. There was no appeal to goals or end-directed action. Right? Wrong.

Evolutionary theory is Aristotelian. Practitioners use teleological language to describe how evolution works, ad nauseam. When evolutionists explain that the bat’s specialized airflow sensors evolved in order “to guide” motor behaviors, they are invoking an end- or goal-directed process. If nervous systems evolved “to accommodate” various capabilities such as flight, then evolution is Aristotelian.

Now the usual explanation for the teleological language, which is rampant amongst evolutionists, is that “we didn’t actually mean it, we’re just being lazy.”

In peer-reviewed papers?

No, evolutionists are not being lazy. Not this lazy. This is how they think about the evolutionary process. It performs actions in order to achieve goals.

Consider this week’s example, a study of embryonic development in vertebrates and how neural crest cells maintain their flexibility or pluripotency. The mystery is that these cells are able to give rise to various types of cells past the embryonic stages where most cells have lost that capability and instead are committed to a particular cell type such as skin, muscle or bone.

The explanation is that these cells evolved that way. Such explanations are given as though they advance the science.

But this adds nothing to the science. Explaining away an unexpected observation as “well evolution did it” is a cheap short-circuiting of the scientific method. It is a meaningless multiplying of entities which Occam warned us never to do and introduces explanations which themselves are in need of explaining.

As Descartes put it: “If you find it strange that … I do not use the [Aristotelian] qualities called ‘heat,’ ‘cold,’ ‘moistness,’ and ‘dryness,’ as do the philosophers, I shall say to you that these qualities appear to me to be themselves in need of explanation.”

This evolutionary reasoning—if it can be called reasoning—shuts off the search for how nature works—the main duty of science. Instead of figuring how embryonic development works it is simply ascribed to the contingencies of history. The underlying reasons for the design, which in its inexorable march of progress science will eventually uncover, are ignored. Evolutionists are, as they say, being lazy.

But that’s not the worst of it.

The constant teleological drumbeat in evolutionary theory not only obviates the scientific method, it replaces it with cacophony of serendipity. The evolutionary literature is chocked full of intricate, complicated, just-so stories that would put any soap opera to shame. All kinds of intricate events take place, leading to complex new creations which are then crucial to the next step in the plot.

This week’s paper on neural crest cells, for example, finds that after these fascinating and incredible cells were produced by evolution, they then became the crucial player in evolution’s construction of major new vertebrate designs. Here is how evolutionist Carole LaBonne, the study leader, explained it:

Neural crest cells never had their potential restricted at all. We believe a small population of early stem cells were set aside, so that when the time came, their immense developmental potential could be unleashed to create new features characteristic of vertebrates.

Early stem cells were set aside so that when the time came their immense developmental potential could be unleashed to create new features? This is Aristotelianism on steroids and the serendipity is deafening.

When you see a theory consisting of a long sequence of special explanatory devices you know it isn’t about science.

Here is Another Retrovirus With an Important Function

Don’t Just Assume It’s Junk

The more that evolutionists claim nature is full of junk, the more that science finds uses for the junk. An intriguing example are the retroviruses which, for several years, have been found to have various functions. Yet another retrovirus function was published last fall in a study out of Canada. This retrovirus works with several proteins in human embryonic stem cells
and without it the stem cells lose their key functionalities.

Human endogenous retrovirus subfamily H (HERVH) is a class of transposable elements expressed preferentially in human embryonic stem cells (hESCs). Here, we report that the long terminal repeats of HERVH function as enhancers and that HERVH is a nuclear long noncoding RNA required to maintain hESC identity. Furthermore, HERVH is associated with OCT4, coactivators and Mediator subunits. Together, these results uncover a new role of species-specific transposable elements in hESCs.

As with previous human retrovirus examples, this finding forced evolutionists to hypothesize that the retrovirus, unbelievably, played a crucial role human evolution. As one report explained:

According to the study's lead author, Xinyi Lu, a postdoctoral researcher in Ng's laboratory, the emergence of the regulatory activities executed by HERV-H could represent an important step in the evolution of our early ancestors. "HERV-H first integrated into the primate genome around 45 million years ago and is only found in the primate genome," says Lu, "and so it may contribute to some of the differences between primates and other mammals."

How curious this is. A retrovirus is supposed to have evolved, and then it just happened to play an important role in the construction of humans. This is yet another example of the incredible serendipity that evolutionists envision at work in their theory. Do they ever wonder at the likelihood of a retrovirus just luckily fitting in to the evolutionary process, and serving in an important role in the production of increasingly complex organisms?

With evolution, science becomes not a search for how nature works, or what likely occurred in the past, but rather bizarre, unlikely tales that cannot be proven wrong.

Religion drives science, and it matters.

Evolution Professor: We Evolved to be More Complex

Serendipity and Aristotelianism

We recently saw how evolutionists are elaborating on what they view as an evolutionary arms race within our genome. Rival elements battle it out as transposable elements invade and repressors seek to shut them down. The transposable elements are “continually evolving to escape repression,” while the repressors adjust and find new ways to defeat the transposable elements. It is “a never-ending race” according to one evolutionist. The backstory here is the on-going historical feud between those who view nature as perfect and those who view nature as evil. In the eighteenth century, for instance, the English natural theologians presented a decidedly optimistic, rosy version of the world, to which Hume responded that “A perpetual war is kindled amongst all living creatures,” and that nature is so arranged so as “to embitter the life of every living being.” So who is right? The answer, of course, is that both are right. Nature is both wonderful and dangerous at the same time. As usual the heresy is not in recognizing these obvious truths, but in emphasizing and dwelling on one side of the spectrum, to the exclusion of the other. Creation and Scripture—general revelation and special revelation—are studies in contrast. Science requires recognizing both sides of the contrast, and keeping them both in view together. Show me a cult, either religious or scientific, and I’ll show you people who are fixated on one end of a spectrum. The result is a lopsided theory that makes no sense.

Consider the genomic arms race idea, for example. First, it requires rapid evolution of astonishing complexity. Not likely. Second, it calls upon a monumental amount of serendipity. Humans and frogs have “basically the same 20,000 protein-coding genes as a frog, yet our genome is much more complicated, with more layers of gene regulation.” How did that happen? Those astonishing levels of sophistication and subtlety in the human genome arose with the help of these invading transposable elements. The incredible regulation machanisms that arose to repress them, just happened to take on other roles as well. This resulted in primates and ultimately humans. Really? Evolution just happened to produce transposable elements, and they then became evolutionary mechanisms? In other words, evolution created evolution. As the report summarizes, “repressor genes that originally evolved to shut down jumping genes have since come to play other regulatory roles in the genome.” That was lucky.

Furthermore, to understand and communicate this story, evolutionists dive deep into the waters of Aristotelianism. It is the ultimate internal contradiction, for the theory that is supposed to represent the triumph over teleology is, itself, immersed in it. Consider these examples:

a transposable element changed to become expressed and replicated itself throughout the genome

The way this type of repressor works, part of it binds to a specific DNA sequence and part of it binds other proteins to recruit a whole complex of proteins that creates a repressive landscape in the genome. This affects other nearby genes, so now you have a potential new layer of regulation available for further evolution.

the transposable elements are themselves continually evolving to escape repression

This paper shows how important it is to integrate computational and experimental approaches to fundamental scientific problems, such as how and why we continuously evolve to be more complex.

For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions.

KZNF genes rapidly evolved to repress these two distinct retrotransposon families

evolved earlier to repress the primate L1 lineage

followed by mutations in these retrotransposons to evade repression

Evolving to escape repression? Changed to become? We evolved to be more complex? This is not science, this is story telling. We need to stay with the evidence.

Evolutionist: “In a Very Real Sense, Our Species Invented Itself”

The Aristotelianism Just Keeps on Getting Stronger

Evolution is a narrative, not a law-driven theory, and narratives are all about plot lines, conflicts and resolutions, good guys and bad guys, value-laden themes, motives, goals, objectives and so forth. These elements repeatedly appear in the evolution literature. For instance, in evolution there was at one point a “push” toward smaller dinosaur sizes, and the smaller sizes in dinosaurs helped to “trigger” a host of different traits. A wing-like surface area would have developed “to help glide” from tree to tree. After all, dinosaurs “were experimenting” with flight in various modes and finally “made the crucial leap” to powered flight, and so birds “were born.”

Cells worked together for a common goal of reproducing more cohesive units, and thereby worked in a concerted way toward increasing their fitness.

Conserved non-coding DNA was the result of regulatory innovations.

The genetic code emerged to avoid random protein sequences.

Small-headed snakes rapidly evolved “to probe eel burrows.”

Oxytricha trifallax, a profoundly complex single-cell organism, was “one of nature’s early attempts to become more complex.”

The brittlestar’s distributed and multifunctional vision system was “designed to minimize spherical aberration and birefringence.”

New proteins evolved because “Nature probably uncovers new topologies in order to fulfill new functions, and optimizes existing topologies to increase their performance.”

The amazing leaproache “evolved to do what grasshoppers do—jump between stems.”

The harp sponge evolved its elaborate candelabra-like structure “in order to increase the surface area.”

The list goes on and on and these are but a tiny sampling of the teleological Aristotelianism one finds in the evolution literature (see more details of these examples here, here and here).

So we were not too surprised to see Peter Corning’s 2013 paper on how behavior has shaped evolution. Corning explains that the behavior of organisms has had a significant influence in the evolutionary process of creating new species. There has been, Corning explains, “a flood of research on how behavioral influences contribute to the ongoing evolutionary process but “the theoretical implications of this paradigm shift still have not been fully integrated into our current thinking about evolution.”

Indeed. Gone is the evolutionary notion of random variation subject to natural selection, otherwise known as “chance and necessity.” Instead, organisms, whose behavior is driven by goals, play an active and major role in evolution. Simply put, as Corning concludes, “our species invented itself”:

Behaviour has a purpose (teleonomy); it is ends-directed. Living organisms are not passive objects of ‘chance and necessity’ (as Jacques Monod put it). Nor is the currently popular concept of phenotypic plasticity sufficient. Organisms are active participants in the evolutionary process (cybernetic systems) and have played a major causal role in determining its direction. It could be called ‘constrained purposiveness’, and one of the important themes in evolution, culminating in humankind, has been the ‘progressive’ evolution of self-determination (intelligence) and its ever-expanding potency. I call this agency ‘Teleonomic Selection’. In a very real sense, our species invented itself. For better and worse, the course of evolution is increasingly being shaped by the ‘Sorcerer's Apprentice’. Monod's mantra needs to be updated. Evolution is a process that combines ‘chance, necessity, teleonomy and selection’.

There is, as always, a problem in this Greek drama. Those organisms, and their behaviors, had to be created by evolution. In other words, evolution just happened to create incredibly complex biological agents with incredibly complex behaviors which then just happened to be crucial influences on the evolutionary process. In short, just as Corning concludes that our species invented itself, we must also conclude that evolution invented itself.

Whereas evolution once called on fairly basic mechanisms such as random variation, it now is at the other end of the spectrum, calling on diploid genetics, horizontal gene transfer, etc., and now human behavior—the most complex mechanisms one can imagine. And those mechanisms must have been created by evolution. Perhaps it is time for a Deus ex machine, for this level of serendipity is beyond silly. At least evolution is entertaining.